Current Research and Scholarly Interests
Our laboratory uses genome-wide methods to uncover alterations that drive cancer progression and metastasis in genetically-engineered mouse models of human cancers. We combine cell-culture based mechanistic studies with our ability to alter pathways of interest during tumor progression in vivo to better understand each step of metastatic spread and to uncover the therapeutic vulnerabilities of advanced cancer cells.

Current Research and Scholarly Interests
He is a health policy and outcomes researcher whose work has focused on children's health; health-outcomes disparities by race, ethnicity and socioeconomic status; the interaction of genetics and the environment as these factors influence child and maternal health; and the impact of medical technology on disparities in health outcomes.

Bio
Tim Witney is a Post-Doctoral Scholar and member of the Molecular Imaging Program at Stanford University.

He joined Professor Sanjiv Sam Gambhir's lab at Stanford in 2013, building on 3 years of postdoctoral research in biomedical imaging at Imperial College London and doctoral training at the University of Cambridge. His research interests include the discovery and development of new PET and MR methods to image tumour metabolism and the down-stream effect of targetted therapeutics. The development of a new generation of molecular imaging techniques will focus on early cancer detection, assess the efficacy of novel and preexisting cancer therapeutics and help describe the fundamental biological mechanisms that drive treatment resistance.

He was a finalist in MedImmune's 2009 Oncology Competition and has previously worked as a Research Biologist at GE Healthcare.

His blog on cancer imaging can be found at http://cancerimaging.blogspot.co.uk/

Current Research and Scholarly Interests
Our goal is to define targets for cancer therapeutics by identifying alterations in signal transduction proteins. We first identified a naturally occurring mutant EGF receptor (EGFRvIII) and then delineated its unique signal transduction pathway. This work led to the identification of Gab1 followed by the discovery that JNK is constitutively active in tumors. We intiated using altered proteins as the target for vaccination, where an EGFRvIII based vaccine appears to be highly effective.

Current Research and Scholarly Interests
My research interest is focused on investigating the molecular networks that underlie cancer stem cells and designing therapies that selectively target these cells, thereby eliminating a cancer's potential for regrowth.

Bio
I am a graduate of the Harvard School of Public Health with a dual-doctorate in molecular / genetic epidemiology and environmental health. During my doctoral training, I developed extensive skills in quantitative analysis, epidemiological study design, and causal inference in observational studies. However, I am best described as a genomic trauma specialist focusing on the relationship between molecular markers, telomere dynamics, and risk of chronic diseases.

My career in biological research began at the British Columbia Cancer Agency under the guidance of Dr. Keith Humphries, a world renowned expert on the genetics of hematological disorders. It was in the Humphrie’s laboratory that I developed a strong foundation in molecular genetic techniques which served as a primer for the rest of my career. Subsequently, I became research laboratory manager for Dr. Immaculata De Vivo, a pioneer in molecular epidemiology at the Channing Division of Network Medicine at the Brigham and Women’s Hospital. Not only did I hone my expertise in molecular biology, but also received extensive training in the burgeoning field of molecular and genetic epidemiology. I used a three-pronged paradigm in my research to combat cancer; understanding genetic and biological susceptibility, prevention by attenuating modifiable risk factors, and treatment of underlying causative factors. With respect to genetic susceptibility, my projects focused on functional characterization of polymorphisms which predisposed women to endometrial cancer. With respect to attenuating modifiable risk factors, we studied how smoking and other lifestyle choices affect cancer risk. With respect to treatment of underlying disease, I studied how a novel therapeutic molecule called dichloroacetate induces cell death in a panel of endometrial cancer cells.

My doctoral thesis focused on the effect of airborne particulate matter on telomere length, mediated through chronic inflammation and global DNA methylation. Furthermore, I investigated gene-environment interactions with respect to endometrial cancer risk in the Nurses Health Study. My interest in predictors of chronic disease is not limited to only biological and environmental factors, but also social factors such as exposure to racism and early-life adversity in susceptible populations.

Current Research and Scholarly Interests
Current interest centers on the application of statistics to problems arsing from biology. We are particularly interested in questions concerning gene regulation and signal transduction.

Current Role at Stanford
Working within the School of Medicine, I am developing solutions for the Stanford Bone Marrow Transplant, Lymphoma, and Cancer Institute Research Databases

My Stanford Projects:

- Stanford Cancer Center Research Database (SCIRDB)Developed a web-based platform to integrate data from the Stanford Cancer Institute (EPIC/Clarity), Stanford Tumor Registry, STRIDE (Tissue Bank & Pre-EPIC Data), and several other systems into a "one-stop shop" for data analysis and annotation by cancer researchers. This cohort-driven system allows users to focus on their patients of interest and provides free-text search of all their notes, reports and narratives as well as a timeline-based view of all events for a patient. Easy exports allow for data analysis in biostatistical tools and the system can perform complex analysis using the open-source R statistical software as a service.

- Lymphoma Program Project (LPP)Rearchitected an existing legacy database system that tracks Stanford's Non-Hodgkins and Hodgkins Lymphoma cases back to the late 1960's. Enables clinicians to track diagnosis, courses of treatment, long-term follow-up, and clinical responses to the diseases.

- Bone Marrow Transplant ProgramDeveloped replacement web-enabled database based on legacy system in place since 1980s that enhanced data capture abilities by leveraging data feeds from BMT Clinic and Stanford Hospital. Also enabled electronic form submission to national transplant databank via XML-based web-services.

- Stanford Asian Pacific Program in Hypertension and Insulin Resistance (SAPPHIRe)Provided on-going maintenance for the project by uploading data, generating reports for statistical analysis and modifying table schema to incorporate new measurements such as creatinine.

- GenePad ProjectDeveloped a web-based tool for quality assurance of scanned form data that allows users to view scanned input and validate it before storing it into final database tables. The tool dynamically configures itself by examining the structure of the database.

Current Research and Scholarly Interests
I am interested in the epigenetic reprogramming of DNA methylation during early mammalian preimplantation development. Early mammalian development is characterized by dramatic epigenetic changes. Upon fertilization of the oocyte with the sperm, the maternal and paternal genomes of the zygote are extensively reprogrammed to ensure the development of a totipotent potential. During this period of epigenetic reprogramming, DNA methylation (5-methyl-cytosine, 5mC) of paternal and maternal chromosomes is erased and reset during formation of the blastocyst. Interestingly, in mouse zygotes, the paternal genome becomes actively demethylated, as judged by immunofluorescence with antibodies against 5mC and bisulfite-sequencing data. Since the discovery of active DNA demethylation many scientists were trying to identify the putative “DNA demethylase” and a lot of candidate enzymes and pathways have been suggested and disproven. The identification of the enzymatic conversion of 5mC to 5-hydroxymethyl-cytosine (5hmC), 5-formyl-cytosine (5fC) and 5-carboxyl-cytosine (5caC) by Tet1-3 enzymes sheds new light on this process.However, the analysis of epigenetic reprogramming in mammals is mainly focused on the mouse model and little is known about human embryonic development. Understanding the basic molecular mechanisms of human epigenetic reprogramming will impact human reproductive health and the generation of pluripotent stem cells